of the impairment time course. In particular, the performance scores were already showing recovery from peak impairment 2 h post-drug ingestion, although quazepam's potent N-desalkylflurazepam metabolite has been found to maintain a maximum plateau level from 2 to 24 h. according to a random Latin square design balanced for order of drug administration. The drug effects on the performance of motor coordination and cognitive tasks were monitored for 7 h following drug ingestion. The results did not indicate any differential effects on cognitive-neuromotor performance for the BZ1 specific quazepam and 2-oxoquazepam compared with the BZ1, BZ2 nonspecific N
-after drug plasma levels, sleep efficiency, next-day mood, and performance. Patients in the four treatment groups received either flurazepam 30 mg, flurazepam 15 mg, midazolam 15 mg, or placebo. Plasma drug concentrations of N-desalkylflurazepam and midazolam were measured by electron-capture gas chromatography. Values of midazolam during the 14-day study were at or near the sensitivity limit of the assay and were not used in the calculations. Levels of N-desalkylflurazepam increased as expected during the 14 days. Mean level for the high-dose flurazepam group was approximately twice that of the low-dose group. The main consistency in the correlations, which were found on days 13 and 14, was that the high-dose desalkylflurazepam concentrations had a negative correlation with two independent
the two shapes appeared the same or different and his reaction times were simultaneously recorded. Neither benzodiazepine influenced the latencies of any of the sensory and late EP components. Flurazepam's long-acting metabolite, N-desalkylflurazepam, reduced the amplitudes of all the EP components suggesting a somewhat general mode of action. This was not the case for lormetazepam. N-desalkylflurazepam , were reduced considerably more after flurazepam administration than their counterparts recorded from the occiput. This observation points to the possible existence of at least two separate sources of the N200-P300 complex with different affinities to the N-desalkylflurazepam. The flurazepam-induced amplitude reduction observed for VEPs to gratings may reflect an attenuation in the detectability
not interfere with sleep, blood was drawn by an indwelling catheter from a large arm vein. Plasma concentrations of quazepam and its two major plasma metabolites (which are also active) 2-oxoquazepam and N-desalkyl-2-oxoquazepam (N-desalkylflurazepam) were determined by specific GLC methods. Kinetic analysis was by a two-compartment open model with first-order absorption/formation kinetics. Quazepam
of sleep EEG changes, especially during the latter part of the 37-night treatment period. Both groups significantly increased sleep spindle rate and decreased delta count per minute. The patterns of withdrawal were also similar. Plasma levels of N-desalkylflurazepam were not significantly related to the magnitude of EEG changes.